# Synaptic Plasticity in Neurodegenerative Diseases: Impact of Exercise as Promising Therapeutic Tool

## TL;DR

Exercise can help protect brain function in neurodegenerative diseases by improving synaptic plasticity and reducing inflammation.

## Contribution

This paper highlights exercise as a promising therapeutic tool for neurodegenerative diseases by targeting synaptic plasticity and neuroinflammation.

## Key findings

- Synaptic plasticity dysfunction underlies neurodegeneration and neuroinflammation.
- Exercise can counteract synaptic plasticity decline and maintain neuroimmune homeostasis.
- Exercise enhances neuroplasticity by targeting molecular mediators involved in neurodegeneration.

## Abstract

What are the main findings?
Synaptic plasticity dysfunction is the basis for neuroimmune inflammation/neurodegeneration.Exercise can counteract synaptic plasticity decline/neuroinflammation and maintain neuroimmune homeostasis.

Synaptic plasticity dysfunction is the basis for neuroimmune inflammation/neurodegeneration.

Exercise can counteract synaptic plasticity decline/neuroinflammation and maintain neuroimmune homeostasis.

What are the implication of the main findings?
Exercise should be included as a promising intervention for supporting and preserving neuroplasticity

Exercise should be included as a promising intervention for supporting and preserving neuroplasticity

Neurodegenerative diseases are distinguished by synaptic dysfunction and chronic neuroinflammation, which accelerate neuronal loss and impair network resilience. Synaptic plasticity, that is, the ability to adapt to changes, is progressively lost. This ability is part of hormesis, an adaptive biphasic response, nowadays acknowledged as a promising tool in chronic degenerative diseases, since it offers a framework for personalized interventions. Growing evidence supports exercise as a powerful approach for managing neurodegenerative disorders, due to its capacity to enhance neuroplasticity through the direct targeting of the biomolecular processes involved. Indeed, regular exercise can drive many molecular mediators and signals toward neuroplasticity improvement, potentially slowing neurodegeneration. This narrative review focuses on exercise as a promising therapeutic approach in neurodegenerative diseases, based on its ability to shape synaptic plasticity at the molecular level. Some biomediators involved in synaptic plasticity function/dysfunction and neuroinflammation/neurodegeneration are addressed as therapeutic targets of exercise, and different exercise regimens are discussed as specific therapeutic interventions to contain the burden of some neurodegenerative conditions. Some clinical trials including exercise in the treatment of neurodegenerative diseases are summarized. Since no definitive disease-modifying cure exists for these illnesses, exercise’s ability to shape synaptic plasticity emerges as a highly attractive therapeutic approach.